February 13, 2025 • 56 mins
Discover the exceptional benefits of vitamin K2, especially its form MK-7, as Dr. Brad McEwen, a naturopath and nutritionist, joins us to reveal the nutrient's essential roles in our health and wellness.
Gain insight into the unique structural and functional differences between vitamin K1 and K2 and how these contribute to our bodily functions, from bone health to cardiovascular wellness. Delve into the potential positive impact of vitamin K2 on chronic conditions.
This episode unpacks the incredible ways vitamin K2 serves as a director of calcium in our bodies, guiding it to strengthen our bones and keep our arteries clear of calcification. We'll explore the critical synergy between vitamin K2 and vitamin D3 for chronic disease prevention and the science behind the activation of bone mineralization proteins.
Dr. McEwen shares valuable knowledge on the importance of monitoring vitamin K2 levels for optimal health and why it's imperative for practitioners to stay well-informed through ongoing research.
About Dr Brad:
Dr Brad McEwen, PhD, is a leader in preventive and personalised health, particularly in the area of cardiometabolic health and mental and cognitive health. He is an award-winning naturopath, nutritionist, herbalist, educator, researcher, and mentor with over 24 years of clinical experience. He has a PhD from the University of Sydney, a Master of Health Science (Human Nutrition) and a Master of Public Health from Deakin University, among other qualifications in nutrition and sports medicine. He has a passion for teaching and has been educating in nutritional and naturopathic medicine and the health sciences for over 20 years. He has extensive experience in presenting seminars, webinars, and at conferences nationwide and internationally,
Brad has a passion for research. He has published numerous original research and review articles in peer-reviewed journals. He is a peer reviewer for international journals. His research interests include the effects of diet, nutrition, and lifestyle medicine on cardiovascular disease, cardiometabolic syndrome, depression, anxiety, polycystic ovary syndrome, endometriosis, cognition, stress, type 2 diabetes, and chronic disease.
Connect with Dr Brad:
Website: https://www.cmgrouponline.com.au/
Shownotes and references are available on the Designs for Health website
Register as a Designs for Health Practitioner and discover quality practitioner- only supplements at www.designsforhealth.com.au
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DISCLAIMER: The Information provided in the Wellness by Designs podcast is for educational purposes only; the information presented is not intended to be used as medical advice; please seek the advice of a qualified healthcare professional if what you have heard here today raises questions or concerns relating to your health
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:10):
Music.
This is Wellness by Designs,and I'm your host, andrew
Whitfield-Cook.
This is Wellness by Designs andI'm your host, andrew
Whitfield-Cook.
Joining us today is Dr BradMcEwan, a PhD naturopath and
(00:30):
nutritionist who works with theComplementary Medicines Group,
and today we'll be discussingall about vitamin K, mk7.
Welcome to Wellness by Designs,brad.
How are you?
Speaker 2 (00:43):
I'm very well.
Thank you very much for theintroduction.
How are you?
Speaker 1 (00:46):
I'm great mate.
Very good Now.
First of all, we need todifferentiate between the
vitamin Ks, because it's one ofthose much misunderstood
molecules, particularly inmedical circles, who still don't
realise that there's more thanjust vitamin K.
So can you take us through thedifferent side chains, the
(01:08):
different molecules?
What is vitamin K and what isvitamin K2?
Speaker 2 (01:14):
So, first off, I'd like to start by saying I'm very
excited about doing thispodcast and I believe that you
know everyone should have havesome.
Everyone should have somevitamin k2.
And, to finish off with that,thank you very much for all your
attention.
Sorry, just a side joke.
So the exciting thing aboutexciting thing about vitamin k2,
(01:36):
as what you're saying, andrew,is, it's a very wide field of
information and if you think ofit in a way as, yes, there's
vitamin K1, vitamin K2, but whyshould everyone be having some
and what is so special about it?
And one of the areas I want youto think about is let's start
back at the beginning looking atstructure, function,
biochemistry.
Put that in your mind as we gothrough today's journey I'm
(01:59):
going to say today's a journeythrough vitamin K2, because
we're going to cover a widerange of different areas.
So, as we go through, think ofstructure, function,
biochemistry and what's linkingall these things together,
because if you understand that,you'll have a better
understanding of, you know,health and nutrition and sort of
naturopathic medicine ingeneral.
So when we start thinking about, you know, vitamin K, vitamin
(02:22):
K2, cetera.
What is it?
So the two main ones we look atis vitamin K1 and vitamin K2,
named normally in numericalorder, as, like the B vitamins,
it sort of goes in order of whenthey're found.
So one thing I want you tothink about is vitamin K1 has a
vital side chain, so it's sortof like a lipophilic side
(02:43):
structure and that's its maindifferentiating point, while
vitamin K2 has more like acarbon chain, carbon bonding
type of effect, where we'relooking at sort of these repeat
molecules, and that's the maindifference structurally between
the two.
I know it sounds sort of simpleOne's more of a lipophilic and
one is more of a sort ofcarbon-based structure.
(03:05):
But that actually helps benefitthe differentiator.
Two of how they work.
And we always see things likeyou know what is the difference
between minoquinone 4,minoquinone 7, minoquinone 10?
There's all the way from sortof number 2 to number 14.
And that's all based on thenumber of side chains.
So there's your biochemistry.
(03:25):
Very easily, it's just a simplething.
As in, how many side chainsdoes this have?
And in this case, menaquinone 7,which is the focus of what
we're talking about today, has 7.
So I want you to think sort ofyou know, how do we get this?
Where does it come from?
So vitamin K2, particularlymetaquinone 7, is formed in the
(03:46):
gut.
It's formed in our bacteria, sowe can actually manufacture
part of it ourself and infermented foods, of course, from
the bacteria of the fermentedfoods.
So that sort of takes us backto you know, it all happens in
the gut effect.
You know how we talk a lotabout naturopathic medicine is a
lot of symptoms and systems, Ishould say, work from the gut
(04:06):
out, inside out.
So if we keep that in mind,that's a very big area.
If we have good digestivehealth, we'll have better
digestive health related to ourvitamin K2 metabolism,
particularly in Medicare 7.
So I want you to start thinkingabout comparing the pair if you
think about this.
So Medicare 7iQ7 is, we'relooking at, absorbed in the
(04:28):
large intestine, while vitaminK1, phylloquinone is actually
absorbed into the smallintestine.
So it's sort of like the smalldifferences.
To start with, and as we gothrough the different processes,
vitamin K1 and vitamin K2 areboth sort of absorbed and
utilized into our chylomicrons,into our ldl cholesterol as well
(04:49):
.
So we always tend to think ofldl cholesterol as being, you
know, the bad guy causes allthese problems.
But I try and think, hang on,ldl actually does play a role on
the body.
It's very useful for, um youknowuble vitamin carrying, such
as K2, but also other nutrientsas well, throughout the body, so
it actually has a wider role.
(05:11):
So if you think about this,vitamin K2 and K1 gets absorbed
in our gut, gets attached andenveloped, I suppose, by the
chylomicrons and depositedthroughout the body, and
particularly with K1, it goesinto the body, gets picked up by
the VLDLs and gets taken backto the liver where it tends to,
let's say, live its life.
(05:32):
Vitamin K1 particularly does alot of functions in the liver.
The difference with vitamin K2is it tends to utilize the LDLs
a lot more easily and transportto what we call the extra
hepatic tissues that are outsidethe liver.
So vitamin K1 stays inside theliver.
Essentially, after absorption,vitamin K2 goes throughout the
(05:53):
body, and that's what makes itdifferent as part of our
clinical side that we'll talkabout later.
The other thing that's excitingabout vitamin K2 is it crosses
the blood-brain barrier.
So that's something we canstart thinking about later on
when I talk about plaque formingand crystal forming conditions
think of alzheimer's or multiplesclerosis, etc.
(06:13):
That it can actually havegreater benefit in.
So everyone always thinks withk2 is blood and bones, which is
good good to think that way, butwhat we'll be talking about in
this podcast is, you know, alittle bit more than that yeah,
okay.
Speaker 1 (06:30):
So a couple of questions straight off the bat.
If we're talking about in uhmk7 being incorporated into the
ldl molecule, does it have anyprotective effects there, like,
for instance, ubiquinol does,protecting the LDL particle
against oxidation and thereforefoam cell production?
(06:51):
Do we have any evidence thatMK7 has that sort of protection
against atherogenic molecules?
Speaker 2 (07:00):
It's an area I haven't looked into yet but it's
quite exciting because I likethe ability of how vitamin K2
does have that antioxidanteffect and cell protective
effect.
And if you were to combine itwith ubiquinol, tocotrienols,
for example, and other similarantioxidant molecules, you could
predict from small, dense LDLslike the golf ball effect of it
(07:22):
smashing into the arterial walls.
Like the golf ball effect of itsmashing into the arterial
walls.
So from my thinking of goingback to, like I mentioned
earlier, our structure functionbiochemistry, short answer is
yes, I think from what weunderstand, it will do that.
It's not an area I've lookedinto but I will now.
But it's something that I thinkwill actually make a big
difference of our understandingof how vitamin K2 does that work
(07:44):
.
Speaker 1 (07:45):
Yeah, and another one .
Sorry, brad, to go straight offthe bat, because you piqued my
interest, and that was whenwe're talking about being
incorporated or helping theliver.
Do we have any evidence yetthat vitamin K2 MK7 might be
(08:09):
beneficial in conditions,metabolic conditions like, um
well, we used to call itnon-alcoholic fatty liver
disease, but we realized thatthere was too many people
drinking not having none, um, soI think the acronym is now
massaled.
Is that right m something?
Speaker 2 (08:21):
like that.
Yeah, there's a lot ofmetabolic associated.
Speaker 1 (08:25):
Metabolic associated don't know what the host in
their liver disease muscle.
Um yeah, I think the acronymschange, but do we have any
evidence yet that MK7 is abenefit in those conditions?
Speaker 2 (08:40):
not that I've seen particularly like related to
what you're saying, but if youlook at the wider aspect of how
non-alcoholic fatty liverdisease or fatty liver disease,
cirrhosis or any of these liverdiseases work, the short answer
again is yes, I believe it willactually have great benefit in
that area because it is workingthrough the regulation of
(09:01):
cholesterol metabolism,antioxidant, anti-inflammatory
pathways, calcification pathways, which I'm about to talk about.
So I do think that we are goingto see more benefit in that
research.
The main sort of focus ofresearch of K2 that we'll be
covering has been extrahepatic.
They haven't really beenlooking at the liver.
But if you think of thevascular system, of course the
(09:25):
liver is very highly containedof vascular tissue, so that's
how part of the filtration unitaffects.
So with my understanding of howit works, it would definitely
greatly benefit.
And there is research withtocotrienols, for example, of
reducing the impact ofnon-alcoholic fatty liver
disease or fatty liver disease,adiposity-based conditions,
(09:47):
which is where there's a newcondition-based ABCD they call
it, which is sort of adipose B,because I can't remember,
because I just thought of itcardiovascular disease, like
they've tried to do like analphabet kind of thing where
each letter means something andit may have an adipose based.
It may be as simple as that.
Um, yeah, right, but it's whereyou start thinking about.
(10:10):
You know, when we do haveadipose tissue, whether it's in
the gut or the liver or aroundthe heart or brain or any other
area, you know it's on fire andit's causing some inflammatory
effects and if you think of anyway that can greatly benefit the
blood flow.
The antioxidant,anti-inflammatory capacity which
vitamin K2 is working in thebackground of, I think it would
(10:32):
greatly benefit in thosesituations.
Speaker 1 (10:35):
Yeah, Okay, so K2, then we've got the different
molecule lengths.
We don't have it here, as is myunderstanding in Australia, the
MK4.
The one that we have availableis MK7, but the molecule lengths
go right up to what?
13 or something.
(10:55):
Is that right?
Speaker 2 (10:56):
So 13 and recently 14 .
So we're finding, you know, alot more research as we go
through, and that's the benefitof you know where we're going
with nutritional medicine andnaturopathic medicine in general
.
So it's not just science.
You know research, of course,but it's how we apply it and
that's where, in the year thatwe're in, it's very exciting to
(11:18):
see a lot more research comethrough.
And there is some MK4 researchout there, so metaquinone 4.
They tend to call it MK, sometaquinone, k2, and then they
break it down into its numbersMK7 is metaquinone 7, metaq7.
So if you think about it, thelower the number, the shorter
the molecule, the longer thenumber.
(11:40):
You know the long chain kind ofeffect.
So if you keep that in mind,that seems to be the way how it
works in the body where the longchain kind of effect.
So if you keep that in mind,that seems to be the way how it
works in the body, where thelonger numbers seem to be more
flexible.
So particularly mk7,metaquinone 7, being in that
mid-range, it is classified as along chain vitamin k.
So I want you to start thinkingabout long chain fatty acids
etc.
It's the same kind of thingwith k2, is you've got different
(12:03):
lengths doing different thingsand a lot of the research is
still based on this sort ofmenoquinone 7 effect because
they're finding that's where ithas the greater effect, because
it seems to have that sort ofmore bio flexibility of the
molecule compared to the longerchain and the shorter chain and
being in the middle it seems tohave that greater effect even
though, as I said, it's stillclassified as a, as a long chain
(12:25):
.
And what I'm thinking about is,as we go through this podcast
and general conversations is, um, there's always new ideas
coming up, like the more wethink about with you know,
biochemistry, and it's a verygood question, you know, with
the length of the structure andhow it works in the body.
Um, again, thinking oftocotrienols with the bifatal
structure and how it works inthe body.
(12:45):
Um, again, thinking oftocotrienols with the biphatal
tail, it's able to move its wayinto the fatty tissue, into the
cell membrane, work antioxidantinside and outside,
anti-inflammatory inside outside, outside in.
So it sort of goes both ways.
We're finding that a lot morewith vitamin k2 now is it's I'll
use the word biphasic, whereit's able to sell signal inside
(13:06):
out and outside in toincorporate a lot of these
changes.
It's quite exciting right?
Speaker 1 (13:12):
yeah, absolutely.
If we're thinking about foodsources, though, like I have not
looked into this at all withregards to chain length, all I'm
aware of is things like nattohence natto farmer, but from the
natto beans with what is abacillus subtilis fermentation.
(13:34):
And then there's cheeses, aswell Swiss cheeses.
I don't know of any othersource and I don't know about if
either, or which foods are morelinked with different side
chains.
Do we have any knowledge ofthat?
Like you said, like we've nowelucidated, a side chain of 14,
(13:58):
so an MK14.
Do we know what foods that'sfrom?
Or is that only from, like,fermentation of bacteria in the
gut?
Speaker 2 (14:06):
Seems to me more from fermentation in the gut, but
also they're finding it in somefermented foods.
So, going back to the natto,which is a fermented food, I'm
thinking, you know, let's jumpahead or back in this case,
things such as, you know,sauerkraut and other just
general fermented foods thathave been around a long period
of time.
We've always used them fordigestive health for centuries
(14:28):
and not really knew how theyworked, and we're still finding
out more and more details aboutfermented foods.
So it makes me think, you know,vitamin K1 is mainly found in
green leafies, for example.
That's one of the main sourcesof it, as we were working on
earlier, and K2 is more infermented foods.
So I'm going to suggest anymajor fermented food with that
(14:52):
sort of bacillus that we werejust talking about.
That seems to be where it'sfound and again in our gut.
So we've got a whole ecologyworking with us or against us in
some cases, that could beworking with metabolising.
Speaker 1 (15:06):
Yeah, okay, so the uses, if we go into, I think the
initial work was done on bones,but then it took a side thing
and was looking atcardiovascular disease.
There was other potential usesas well, depending on the.
What is it the proteins they'reworking on?
Is that right?
Speaker 2 (15:26):
That's right.
So there's a number ofdifferent areas.
So what I was thinking ofbecause when we were originally
talking about this, I wasthinking how can we go about,
you know, discussing thebenefits of vitamin K2 in a
short amount of time, because wecould talk all week about this,
and I was thinking let's gothrough some base health
(15:47):
conditions first and then sortof you know, expand on those.
So the main functions or uses,of course, is improving bone
health.
That's one of the main areasthat they looked at.
You know, reducing fracturerisk there's a lot of research
on that.
Vitamin K2s Everyone alwaysthinks of, you know, calcium and
vitamin D.
That's great because that doeshave a lot of evidence in
(16:07):
phosphorus or phosphates for thebone structure matrix.
But you also need something tosort of direct and work things
out, as in I see vitamin K2 as adirector in a lot of these
areas.
So whether it's blood, bone,other tissue we're about to talk
about and that's what I likeand find exciting about vitamin
(16:28):
K2 is that it is like thedirector.
So we've got other areas suchas blood coagulation, which is
well known.
We keep looking back into that.
Just overall, cardiovascularhealth reducing cardiovascular
risk and mortality, reducingvascular calcification, which
we're going to be talking aboutshortly, reducing arterial sort
(16:48):
of stiffness.
So I want you to imagine thecardiovascular system is like a
hollow tube, as we know, and ifthe hollow tube is flexible and
flowing properly, we have goodblood flow.
Once it becomes sort of stiffand sort of more restricted,
that's when you get yourhypertension's and your
hemorrhages and your vasculardepletion, strokes, heart
(17:09):
attacks, dvt, etc.
Um, metabolic syndrome.
There's a lot more researchthere where vitamin k2 is
working hand in hand withinsulin, which is pretty cool.
So, remember, we're moving awayfrom the original side.
Now, improving chronic kidneydisease, which could also be
related to, you know, type 2diabetes, vascular, yeah, wide
(17:31):
range of different healthconditions.
Of course, with chronic kidneydisease, kidneys are very tough.
You don't normally noticethere's a problem until there's
a big, big problem and, yeah,they don't feel pain too much.
So therefore, they have to bereally large or really small and
sort of I'll use the worddamaged for them to actually
tell you that there's a problemwith themselves.
(17:51):
They're quite tough.
And also just reducingage-related chronic disease
states.
We're finding out.
So, you know, in the lastdecade or so there's been a very
big push for vitamin d3 and youknow vitamin d3 markers and
having x amount of um in theblood, for example, when you do
a blood test should we be alsomeasuring for vitamin k2,
(18:11):
because they work in a similarpattern of chronic disease
prevention or risk reduction?
So I was thinking, sort oftaking us on a bit of a journey
through vitamin k2, if you like,about how it works.
I like stories when it comes tothis because it helps me
remember how it works.
So I want you to start thinkingabout.
(18:32):
You know, vitamin k2 is amultifunctional molecule,
multifunctional nutrient vitamin.
So yes, it starts with thebones that's where we know but
actually starts working in a lotof wide range areas as well.
So it works with a lot of enzymepathways.
So one of them's and I'vewritten down some notes, I
remember how to say them rightgamma glutamyl carboxylase
(18:55):
enzyme pathway, which sort ofworks with glutglutamyl
carboxylase enzyme pathway,which sort of works with
glutamic acid.
So carboxylase is glutamic acid.
So COOH bonds, et cetera.
It seems to work withfunctionality there.
It works with I love this namevitamin K dependent proteins.
I'm like whoever thought ofthat name one day was on fire.
(19:16):
It's like naming Sydney Harbour, sydney Hardney harbour bridge
and sydney opera house andsydney cove.
Like those people get paid bigmoney um great sandy desert
great sandy desert, let's getgum.
Um.
Western australia, northernterritory, south australia.
You did really well.
So.
So this day this person was onfire and called them vitamin k
(19:37):
dependent proteins.
So that really works for me.
So it says what it is.
So one of these particularproteins that works with the I'm
going to call it theglutamization new word of the
day doesn't exist.
Glutamization is osteocalcin.
So we do know osteocalcin.
So if you, whenever you'retrying to understand a word that
(19:58):
you've never heard of and thisis for a lot of our viewers who
may be starting off in theircareers break it down
Osteocalcin, osteo normallymeaning bone calcin, calcium, so
transportation of calcium, andit's synthesized by the
osteoblasts.
The osteoblasts, of course, arebone cells that form and create
(20:19):
things.
This is forming duringmineralization phase of the bone
.
So osteocalcin is veryimportant for bone health and it
binds to the calcium ions andthe hydroxyapatite crystals,
regulating size and shape.
So I want you to imaginebecause we're going to stick
with the bones and start withthe bone matrix One of the main
stages of working on bone matrixis between the ages of eight
(20:41):
and 10.
So, andrew, you and I are alittle bit gone past that point
of ages eight and 10, but we canstill keep working on the
regulation of that because upuntil about the age of 21 to 25,
which is the category that youand I are in it seems to be
still forming and working to getthat sort of solidification for
(21:02):
the rest of our life.
But what I want you to rememberis we're always building,
breaking down.
Nothing is ever set in stone,so to say, because red blood
cell is 120 days, like platelets7 to 14 days, like things are
always growing and developing.
We're growing and developingfrom the moment we're conceived,
(21:24):
the conception of who we are,all the way to the end.
We're always growing anddeveloping in all different
areas.
Everyone always seems mentallyand physically, for example, and
emotionally growing.
But physically the body and thebiochemistry is always growing
and developing.
So our bone is always in thisconstant state of flux, where
it's always moving and it'sregulating and it's changing.
(21:46):
So if you sit down and donothing all day, your bone
mineral density will change,probably go to your buttocks,
because you're sitting on it allday doing nothing.
But if you get up and becomeactive and that's the comment I
made about ages of 8 to 10, upto 11, because you're physically
active and you're actuallyimpacting and pounding on that
(22:06):
bone, and gymnastics and tennisand a lot of these force
activities create that bonestrength.
Swimming doesn't, of course,because it's not weight-bearing
those kind of activities, butanything that's moving,
including just walking, startsthat process.
Swimming doesn't, of course,because it's not weight bearing
those kind of activities, butanything that's moving,
including just walking, startsthat process.
So getting up and moving, andthat's when we start to develop
and those crystals then start toform and our bone starts to
(22:27):
form shape to where it needs tobe.
So, whether it's a long bone ora finger bone or anything else
like that, again, it's the oldif you don't use it, you lose it
kind of mantra that we say witha lot of things.
So if we keep working with thisosteocalcin and this is where
we start to visualize in ourmind that it's sort of creating
(22:47):
a higher affinity to thishydroxyapatite mineral bone
content and it's actuallydriving in calcium and other
nutrients, of course, into thebone tissue and that's what we
really want.
So I want you to start thinking.
This is like a link betweengeochemistry and biochemistry
now.
So I want you to start thinking, because you know geochemistry
(23:09):
is all crystal formation,minerals, et cetera.
So in some cases some peopleare just big walking crystals.
You know, I want you to thinkabout that.
So they've got the bone mineraldensity that's changing.
They may have gout, which iscrystals as well.
So there's a lot of areas thatsort of start thinking about
crystal formation and it's goingto the wrong place.
(23:30):
And osteocalcin, being driven byvitamin K2 and of course
vitamin D3, is working on thisjourney.
So again, we're sort of workingwith visualisation of bone
forming and other tissueutilising it and if we think of
that process we can startthinking about what else happens
.
So osteocalcin then startsworking with energy metabolism,
(23:53):
bone metabolism, endocrinefunction.
So all the different endocrineorgans are starting to become
involved.
So this is all part of ourmetabolic health, because our
bones are metabolic, our bloodis metabolic.
So if you think aboutregulating energy metabolism and
just overall health, that wayit starts working.
And another role which we'lltalk about later is it has this
(24:16):
inhibitory role on angiogenesis.
So angiogenesis, of course, isthe formation of new blood
vessels and we want that tohappen for general health, but
we don't want that to happen incancer, because the generation
of new blood vessels means bloodflow for the cancer cells,
which means growth anddevelopment of them, leading to
cancer formation.
(24:37):
As a brief storyline, it alsoregulates ectopic tissue
calcification.
So ectopic always means awayfrom sort of where it should be.
So in this case we're talkingabout blood vessels.
So there's a wide range ofdifferent areas that we're
working of, just with theosteocalcin side, and it's a
transporter, and we're journe,just with the osteocalcin side
and it's a transporter, andwe're journeying through the
(24:58):
body, and that's what I like.
Start to thinking about allthese vitamins and minerals and
amino acids and everything goingon a journey for our for our
nutritional needs.
Yeah, there's another protein.
There's the matrix GLA proteinthat keeps working with this and
that works with thecardiovascular disease health um
.
Speaker 1 (25:16):
So the matrix GLA proteins.
Brad, can you tell us moreabout those, what they do so?
Speaker 2 (25:22):
again I want you to think about.
You know the terminology matrix, GLA.
So we always talk about thematrix, not the movie, but the
actual matrix in the body, whereit actually works by.
It's like a netting, astructure.
It's hard to explain sometimeswithout using too many hand
motions Cellular matrix, tissuematrix, organ matrix.
(25:45):
It seems to work by, you know,piecing and putting things
together into its cell structure, into its system, and that's
what I find interesting, wherethere's this communication
between cells that are the samecell but also other cells.
The body has this amazingcommunication with itself.
It's just and again, in today'syear we're still finding out
(26:08):
the way, how.
You know, I'm fascinated by howthings work, how we can talk
and think and walk and text anddo all the things all at the
same time.
And it's the body's, you knowmatrix system itself working and
communicating with each other.
And this gla matrix is one ofthose areas and what I was
thinking about, as I mentionedearlier, sort of going through a
(26:29):
bit of a journey into um.
You know, applications of, ofhow we could utilise, you know,
menaquinone 7, K2, and you'vegot to say it's low.
Speaker 1 (26:42):
So the evidence we started off with earlier work by
Thuisson and his group.
What is the evidence nowshowing us?
Because there was some positive, some negative evidence, but
when I looked further it waskind of like what was one of
(27:02):
them there was a positive changein the lumbar vertebrae but a
negative change in the.
Was it radius, radial density,radial bone density?
So it's almost like what youwere talking about earlier about
(27:23):
that need for exercise.
Now I don't know about this.
It was just an interestingthing.
Tell us more about the researchand where it's leading us.
Speaker 2 (27:35):
And that's the exciting thing.
There's a lot of interestingthings that we can really move
into as we go through and I wantyou to think back.
Most people now are becomingmore sedentary over the last few
decades.
We're working more inside, lessactive.
I have my Apple Watch, where Ideliberately have it set, where
I have to get up regularly andmove around so that keeps
(27:58):
circulation going, keep the bodygoing metabolic-wise, and
that's what I'm thinking back to, that study that you're
mentioning, that the lumbarregion is being used more
because you're sitting on it,for example, and you're using it
more as weight-bearing.
While your wrists may be on thedesk, they're not really working
as much.
You may be typing or using themouse, but it's not weight
(28:19):
bearing as compared to yourlumbar.
But if you start exercisingmore and actually moving moving
and grooving and moving around,you start to use that.
That's where some people useweights, you know, like the
wrist weights or just do that.
That's weight bearing still, umyep, so holding it using a
mouse is not weight bearing, butit's sort of like any kind of
(28:39):
activity.
So you know, if you need to getup from your desk and do like
the old 1980s sort of aerobicexercise around the office where
you're punching the air andmoving around, because that sort
of gets things up and movingand then you can add some weight
bearing to that.
Um, so what I'm thinking if Igo through some of the research
(29:01):
that this is leading to, andthen we can have a good
discussion at the end, becauseit's sort of quite exciting
where, where we're going, andpart of that is, of course, you
know, cardiovascular disease.
We're looking a lot morevitamin k2 and quinone 7,
cardiovascular disease.
So one of the areas I mentionedearlier is coronary artery
calcification.
So what is it?
(29:22):
The name it says we're verywell named.
Coronary artery is calcified.
There's a calcification processhappening and it's a very
significant predictor ofcardiovascular disease and
cardiovascular disease risk.
And there's some pioneeringwork in that area where you can
look at calcium scores et cetera.
So one of the areas we've beenlooking at is a deficiency of
(29:44):
vitamin K2 has been linked tovascular calcification, not just
coronary but just overallvascular calcification.
And if you think of it this way,you've got different mineral
deposition, particularly calciumof course, coming from the
calcium hydroxyapatite and wealways say from the bones,
because that's the main storagesite into the vascular system
(30:05):
and then going into the vascularwall because it gets trapped.
So it's like a big centrifugalforce going through the arteries
and then it just gets trappedbecause it's I don't know
heavier.
It's like a big metal goingthrough and it embeds in the
overtime.
As you know, we're talkingabout foam cells,
atherosclerosis etc.
And it starts that calcium youknow process and this deposition
(30:27):
also combines phosphates, otherminerals I'm going to suggest
even heavy metals get involved.
Um, I had a patient many, manyyears ago that had an issue
where no one could work out whatit was and we ended up working
out.
Long story short, the GP camein with her and it was a very
serious case and her files werecan't see my hands, but really
(30:50):
massively printed out, everytest under the sun and I just
about you know bone deposition.
Everything that we sort ofmentioned today and what I found
out was due to her childhood.
There was different heavymetals in the area and that's
what deposited into the tissueand when she moved around, that
tissue left because she didn'thave enough vitamin d, vitamin k
(31:11):
etc.
And then left the bone.
So she had bone pain and thenembedded into her vascular
system, leading tocardiovascular risk.
So that was a good example ofsomeone that had heavy metals as
well and metals combined withmetals.
If we go back to our anions andcations and everything else
like that, they all thebiochemistry all combines
(31:32):
together, leading to thiscomplex which then sat in the
arteries and it can sit in thebasement membrane of the artery,
it can be on the inner or outerside of that membrane, leading
to an inflammatory process, anoxidative process, leading to
like a firestorm in there.
The body tries to heal it bylaying down, you know, fibrin
(31:53):
and different connective tissueto help protect it, putting a
Band-aid down, I suppose.
And then that's when you getyour atherosclerosis, your
plaque formation and then, yeah,your eventual clot in that area
yeah, yeah so it's.
It's a big process.
So if we think about that asoccurring and then we reverse
that process by thinking, okay,we've covered today, thinking
(32:16):
about vitamin K2 and how vitaminK2 works with osteocalcin
crystal deposition, you know themicrocrystalline fibers in the
body, and then you've got yourcell matrix and hydroxyapatite,
we can then start moving anddirecting, as I said, vitamin K2
to me as a director, directingit to the right place.
(32:36):
And it sounds very sort ofstory-like, but that's the way
how a lot of our body works.
It's a big story that's beendirected by our DNA.
The main director, like ourgenetic code, is telling
everything what to do.
So if you think about, you knowthat different process, just
with this calcium, you knowfortification in the coronary
(32:59):
artery and other areas, we canstart thinking about vitamin K2
and how that can benefit.
And there's a lot of differentresearch studies coming out of
you know the really longitudinalstudies.
So these studies have beengoing on, you know, like the
Framingham Heart Study, the LeonStudy, the Nurses Study, the
Health Practitioner Study, theStates Nurses.
(33:21):
There's a lot of researchstudies now where they can look
back over test results from thepast.
There's blood samples from the1940s and 50s and stuff that
they can actually pull out ofminus 80 freezers and actually
test it for new inflammatorymediators that were never around
even 10 years ago.
So they're able to do a lotmore of this research.
And a lot of research isstarting to show not with just
(33:44):
those kinds of studies but otherstudies that vitamin K2
depletion over a period of timehas led to a higher risk of
arterial calcification as wellas just general calcification of
the body in the wrong areas.
Speaker 1 (33:59):
Yeah, this is one of the areas that interests me in
that when looking at theresearch, some of this negative
research was coming out sayingthat vitamin K2, mk7 did not
reduce coronary artery calciumscore.
But I know, clinically it damnwell does.
I had an elderly gentleman whohad a I mean, you'll fall off
(34:24):
your chair when you hear thiscoronary artery calcium score, a
CAC.
The CAC was originallysomething like 5,000.
Now I haven't got the thingsdirectly in front of me, but it
was something in that vicinity,whereas anything over 400 is of
clinical like Huge clinicalsignificance 15% risk.
(34:46):
So this was in the thousands.
Upon taking now I'd have towork out the exact dosage.
Forgive me, but on takingaround about five, six, so let's
say 300, forgive me, forgive me600 micrograms of k2 combined
(35:13):
with 6 000 of vitamin d, plusthere were some other
supplements in there.
Because of the healthconditions of this gentleman, um
, within a six month period, hiscoronary artery calcium score
was reduced by half.
Now that's still massive.
It's still massive.
Speaker 2 (35:35):
It's still 2,500, but that is a significant reduction
in risk.
So this person was leachingbone.
Speaker 1 (35:40):
There was a ticking time bomb, and you're right.
You're right leaching bone.
So it makes me query thequote-unquote evidence where
they say no, it didn't, whenI've seen it work like that.
It definitely does reduce CAC.
Speaker 2 (36:00):
It definitely does.
And dose we'll talk about laterbecause I've got a couple of
points I want to make.
On dose, you know veryspecifically for what you've led
into it very well actually, um,where I'll talk about a couple
of clinical cases as well.
So what I'll do, I'll finishoff this journey and then I'll
(36:20):
talk about the reasons why Ibelieve that those doses do work
in some cases and don't work inothers, because it's sort of,
once we have an understanding ofyou know where this journey is
going, you'll see why certaindoses work, and that goes with
any nutrient, any herb, ofcourse.
So if we continue through ourturbulent journey of our
(36:43):
vascular system forging ahead,you've got arterial stiffness as
well.
So you've got the calcification, you've got the stiffness.
Now, thinking about that personyou just mentioned, they're
turning the stone with thatcalcium score.
It's a very high calcium score,so they're literally turning
the stone.
So arterial stiffness as wellas vascular calcification are
(37:06):
very good predictors ofcardiovascular and overall
health.
I'm going to say so.
A lot of test results can letus know overall health.
So there was a NAPN study whichis quite well known.
There was a double-blind,placebo-controlled, and I've got
to get the number right, I'vegot it in front 244 healthy
postmenopausal women, becauseyou've always got to throw in
(37:26):
the healthy part.
So healthy typically means thatthey don't have the condition
that they are testing for.
So in this case it was 244healthy postmenopausal women.
They investigated the effect ofvitamin K2 at 180 micrograms a
day, which is a standard dosethat we use in Australia.
120 in that and placebo is 124people for three years.
(37:51):
So having any nutritional studyfor a month is pretty good.
Six months is really good.
Three years is really reallygood.
So the longer the researchstudies the better.
So after three years they foundthat K2 improved arterial
stiffness, so the artery is moreflexible.
So sometimes we have to becareful when we say improved,
(38:14):
because the word can go bothways.
So improved arterial stiffness,especially in those with
already high arterial stiffness.
So it sounds quite interestingthat in the people that already
had a high level of arterialstiffness they had a very good
improvement in their blood flowand a reduction in arterial
stiffness at that dosage of 180,versus what you were mentioning
(38:38):
earlier.
They seem to have also had areduction in the GLA protein
matrix area that was seen to behaving a negative impact.
So the flow of calcium in thebody was seen to be more
improved.
So that's just one study.
There are quite many more wecould talk about but due to time
(38:59):
I'm trying to have greaterexamples of each one.
If we go from arterial stiffnessto a wider range health
condition, now called peripheralartery disease or arterial
disease.
So we've gone fromcalcification to arterial
stiffness.
Now we're looking into adisease state name, I suppose,
(39:20):
and this is our journey.
So peripheral arterial diseaseor artery disease is actually
more common than you think.
Arterial disease or arterydisease is actually more common
than you think.
So think of the name peripheral.
So legs, arms, hands, feet, youknow arterial, just arterial
blood flow in disease is justdisease, it's just a condition.
Base Now what they've realisedand worked out with research,
(39:45):
again with longitudinal studies,that a low vitamin K2 status
has been associated withincreased risk of peripheral
arterial disease.
So again, they've been lookingat a lot of studies.
So here's a little study foryou, andrew, sorry about that A
12-year study.
So here we go, 12 years onvitamin K2.
(40:06):
So this was the intake,measuring the intake on a small
number of people, 36,629.
So here we go.
This is where we want the gutsof things now.
So this is where we really seesome really good research come
through.
At the end of 12 years, vitaminK2 intake was associated with a
(40:30):
reduced risk of peripheralarterial disease, with a hazard
ratio of 0.71.
So what this means for theaudience is hazard ratios are
quite interesting to look at.
If you think about it, if youhave a hazard ratio of 1, you're
likely to get it it.
If you have a hazard ratio ofone, you're likely to get it.
If you have a hazard ratio of1.5, you are 50 percent more
(40:53):
likely to get it.
In this case we are 0.71,meaning there's a 29 because you
take that from one, 29 lesschance of this happening.
So that's the hazard ratio.
So I think that's a pretty goodnumber that you know.
Your vitamin K2 status overthat period of time meant you
had a 29% less you know chanceof this happening.
(41:15):
10% for me is great, if youknow what I mean.
Statistically, of course, thehigher or in this case, the
lower the hazard ratio, thebetter.
High blood pressure was measuredin this study as well, because
I measured a lot of differentareas.
Hazard ratio was 59, sorry,0.59.
So there wasa 41.
(41:36):
Reduction in risk.
Type 2 diabetes had a hazardratio of 0.56.
So we're looking at a 44%reduction.
So this is just from the humbleintake being measured of
vitamin K2.
So I think it's quite excitingto see a lot of this base
research being done.
(41:57):
Of course, it's large numberswhen we get this.
But something very interestingfor me, going back to where we
first started, the intake ofvitamin K1 had no association
with reduction of peripheralarterial disease.
Right, and why is that?
Think back to when we firststarted.
Speaker 1 (42:19):
It's different molecule length, but yeah.
Different molecule length, Imean, but not just molecule
length.
There's an answer.
It brings into question thingslike methylation as well.
That's it On treating anexisting condition.
Speaker 2 (42:37):
So the winner of this gets a copy of my book to be
published.
So this is a question for theaudience.
You get a prize, but I'll giveyou the answer as well.
So at the beginning, vitamin K1I mentioned is intrahepatic.
It mainly stays inside theliver.
Vitamin K2 is extrahepatic,meaning it goes out to the
(42:58):
tissue.
So vitamin K1, for example, inthese patients, stayed within
the biliary, stayed within theliver system.
So therefore it would generallynot have an impact on
peripheral arterial diseasebecause it's in the periphery,
while vitamin k2 floats we'lluse the word floats floats
around the body on our ldls andchylomicrons and everything else
(43:19):
like that.
So therefore it's able toachieve its point.
So there's a good example ofwhere k2, being extra hepatic,
is able to do something at thefar ends of the earth, being the
hands, feet, legs and arms.
So goes back to, like Imentioned earlier, structure,
function, biochemistry.
Every time we need an answerthink back.
(43:40):
The answer may not bescientifically proven yet, but
we start to think back in.
What are we thinking about?
It's the physiology, thebackground work.
In this case, that's my answeris k2 did the job because it's
extra hepatic, it went outsidethe liver and did its job rather
than inside the liver.
They didn't do any hepaticmarkers, which would have been
(44:00):
interesting to see, of course,but that's another study to be
done.
I could yeah, well, andrew,both of us could sit down and
write a whole heap of studiesabout what we'd like to research
right now.
It's quite exciting.
Speaker 1 (44:15):
Brad, we spoke earlier about doses.
We need to cover this off.
What doses are appropriate?
Can I quickly ask, by the way,that large study that you were
talking about before, was thatthe Rotterdam study, or was that
a different one?
Speaker 2 (44:30):
It was a different one and I can't remember the
name right now, but it was adifferent one.
No, that's all right.
Speaker 1 (44:34):
They all have different acronyms.
That's fine, can we?
Cover off on dosages, becauseone of the things that's
interesting me is out ofconvenience, we tend to combine
D3 and K2.
Is out of convenience, we tendto combine D3 and K2.
But the more I learn about K2,the more I'm wondering about the
(44:58):
formulae on the market.
Are we wasting the K2?
Are we taking not too much,necessarily, but are we just
wasting the dose?
Should we indeed be taking D3separate from K2?
Speaker 2 (45:07):
That's a very good clinical point when I was
thinking about talking with youabout this.
Is you know how far do we go?
Because I've got notes in mybrain on metabolic syndrome,
peripheral neuropathy,alzheimer's disease, multiple
sclerosis.
There's a whole heap ofdifferent avenues we can go down
(45:28):
to Some of these studies.
Are you know, I'm just thinkingof one now 625 people over 10
years for metabolic syndrome,type 2 diabetes.
There's, you know, a lot ofdifferent avenues and some of
this sometimes comes down toactual dose.
So think about the applicationsports gout, other health
conditions.
It comes down to actual dose.
So think about the applicationsports gout, other health
(45:49):
conditions.
It comes down to dose.
Now, typically the doses we usehere in Australia we are
limited with TGA, so therapeuticgoods administration on doses
of vitamin K2.
So appropriate doses, I'd say,is based on the age group.
So typically adults are 90 to180 micrograms per day.
Based on the research like theNAPN study and a lot of other
(46:12):
research is based on that dosage.
900 to 180 micrograms, sorry,90, not 900.
90, please.
90 to 180 micrograms per day.
Children 10 to 18, becauseclinically they're seen as
children still up until the ageof 18, that's 90 micrograms per
day.
Children 10 to 18, becauseclinically they're seen as
children still up into the ageof 18.
That's 90 micrograms per dayand children less than 10 years
(46:33):
of age is 45 micrograms per day.
So I'll talk about safetyavenues in a moment, because
that's something that you and Ihave discussed over coffee about
.
You know, safety of um,nutrients and nutritional
medicine, etc.
The reason why I think thedoses can be too high is it
(46:55):
comes down to metabolism.
So it's too much of a goodthing is a lot.
So you know there's an oldsaying someone's what is it?
Someone's doses, someone'shealing and someone's poison.
I forget the whole phrase, butthere's a phrase of.
You know it comes down to thedose of the person and if a lot
of research is being basedaround this 90 to 180 micrograms
(47:16):
in in adults, that's that's anarea that we seem to really need
to sort of focus on and keepingin mind.
Is it making the pathways workmore effectively?
Is it, you know, depositingcalcium crystals more
effectively?
It's, it's hard to say becauseI haven't seen a lot of that
toxicology data, for example.
(47:37):
But you start to think abouthow things work.
Are we wasting it with?
You know, combining k2 and d3?
Um, no good.
No, it depends on the formulaand, of course, the person in
front of us, and that's onething I always want to say when
we do podcasts and everything isit's always the person in front
of you.
What is the best dose for thatperson?
(47:58):
And if they need 500 ius ofvitamin d and 90 micrograms of
k2 from your determination,that's the dosage that they need
.
If they need a higher dose of,you know, 1,000 IUs vitamin D3
and 180 micrograms K2, that'sthe dose regime and that's where
(48:19):
a lot of the evidence isshowing.
So going hard and fast is notalways the best way to do it,
because to me, it's trying topush too much through all the
time.
Um, we get excited.
Some studies are very, very highdose and they seem to have the
negative impact because Ibelieve the regulatory pathways
are not able to functioneffectively to make sure we get
(48:41):
the best out of you.
Know what it is.
A good example is waterDehydration.
Water is very bad for you, butso is drowning.
So if you stick to the 30 milsper kilo body weight per day,
that's the NHMRC guidelines forwater, for example, or fluids,
including tea, coffee and don'tget me started on the caffeine
(49:03):
argument, because when you havea coffee you're having caffeine
with water, so therefore itrepletes at the same time.
Um, if you think of it that waythat's the guidelines based on
the evidence then if you startdrinking five, six, seven, eight
, nine I've seen some people do10 liters of water a day and
they're always feeling sluggishand bloated and feeling bad,
(49:23):
it's over hydration.
You're drowning the cells withfluid, you're going against the
concentration gradient.
Sodium, potassium, pumpnutrients, electrical impulses
are not working effectively andyou can get you know fluid in
the brain and die of a stroke orsomething like.
Let's just go serious for asecond.
That's simple, by changing thedose of water.
Now, if we bring that back to amicrogram molecule such as
(49:47):
vitamin K2, and even D3, it's inmicrograms as well.
As I use, these are based ondoses that the body seems to
accept quite well in metabolicstudies and seems to do the
actions that we need.
And I believe that, like withanything, if we smash the body
hard, these channels that thebody has based on evolution from
(50:10):
when we're cave men and cavewomen and didn't eat every day,
and you stored you knownutrients in the body for a
period of time and used them asneeded, we didn't eat as much as
what we do now.
We have food available 24 hoursa day.
The body's mechanism ofmetabolizing and trying to clear
excess you know toxins but aswell as nutrients is not as
(50:33):
functional as what we're pushingin.
So that's what concerns me whenI see very high doses and some
of these studies are actuallygood for us because then we can
see ethically maybe not, butsome high dose studies, we can
see how well something works.
But also get the differentthresholds, because if the
research showed that you knowcurrently 180 is good, but let's
(50:56):
just double it to 360micrograms is a good dose, we
need to then change ourguidelines in australia to meet
that.
But currently, like I, the NAPNstudy and quite a lot of few
studies out there are actuallyshowing that the dosage between
90 to 180 micrograms to adultsseems to do the work.
Speaker 1 (51:15):
I take your point and you know I was thinking about
the risk of possibly not givingenough credence to other
important signals, likeinflammatory signals, for
instance in cardiovasculardisease and calcification.
Brad, there was one more thingI just wanted to ask you and
(51:38):
that was so maximal dose.
We should be really looking atthat 180 micrograms, maybe a
little bit more, depending onwho's in front of you.
I get it, but not going wayhigh, not going too high because
of those other things.
That's right.
There was one study I looked atand even though it was a high
(52:01):
dose and forgive me, I can'tremember the dose there was no
risk of extra.
Let me word that correctlythere was no extra risk of
thrombosis.
So it wasn't acting like avitamin K antagonist, if you
like.
Speaker 2 (52:18):
And that's something that we discussed recently
ourselves, like talking aboutinteractions with pharmaceutical
medications, for example.
Example, and it does alwayscome down to the person in front
of you.
You know what medications arethey taking, what other vitamins
, minerals are they double,triple dosing on things?
You know what kind of effectare we looking at and there are
(52:41):
a number of um studies that wereout there and one of them
showed there was a small studythat showed 45 micrograms a day
decreased the mean value of INRin.
Some patients say yeah, inr isrelated to blood coagulation.
So if you think of it that way,a lower INR means the blood
clots more rapidly and a longeror higher INR means it takes
(53:05):
longer.
So that was one study andthat's the one that tends to be
picked up by people.
There's always certain studies.
So I always turn around and sayread the studies, read the
research.
You know, understand the personin front of you, look at the
genetics, the biochemistry,physiology, etc.
And always be careful what youread.
Read the full journal article,because the abstracts always
(53:27):
look good until you read thefull study.
I'll give a quick examplebecause I know we're running out
of time.
But there's a big omega-3 studypublished many, many years ago.
That said, omega-3 was reallybad.
It leads to thrombosis andclots and hemorrhages and will
kill you.
And I've gone, wow, I did myphd in omega-3.
So I'm freaking out now going,wow, what's going on?
So I look into it and this wasa case study, so I'm going.
(53:50):
Okay, case studies are good.
It's a level of evidence thatwe need.
It was a man in his 70s okay, sohe wasn't young.
He was admitted to hospitalwith hemorrhaging and further
investigation, which was sort ofwritten in a very small part of
the article, was he was outside, fell off a high rung of a
(54:11):
ladder, hit the ground, knockedhis head and he was taking
multiple medications bloodpressure, aspirin, warfarin,
non-steroidalanti-inflammatories and a whole
heap of other things.
But it was the omega-3 thatcaused the hemorrhage.
And I'm like really not thefall, not the medications, but
(54:31):
the actual omega-3 it did it.
So I get a bit triggeredsometimes when, um, I sort of
read some abstracts where, youknow, I believe in all research
is useful, but it needs to befactual research.
And that kind of thing was a bitmisleading because the media
picked it up and went with thatomega-3 causes hemorrhaging when
it can if, given the rightsituation, you're a 70 year old
(54:55):
man who fell off a ladder andlanded on your head, so
therefore there's going to beother consequences of having
that, let alone medications.
So, yeah, always read the fullpaper, look into it deeper.
So now, after this podcast, goand read up all the material, go
and have a look and, you know,nourish your own brain with you
(55:15):
know, information ofbiochemistry and genetics and
physiology, because we'relearning more and more every day
and that's what I love aboutnutritional medicine,
naturopathy and what we dobecause we are learning more and
more and the greater theinformation coming out.
It's fantastic and it's justfor me, it's very exciting the
time and place we're at rightnow with what we could do for
(55:38):
our patients and help each otherout as well.
Speaker 1 (55:41):
Dr Brad McKeown, thank you so much for taking us
through.
This is a big topic, I know,but vitamin K2, MK7 today it's
been great having you on.
Thank you so much for joiningus.
Speaker 2 (55:53):
Thank you very much for having me.
Speaker 1 (55:55):
And thank you everyone for joining us today.
Remember we'll put up as manyshow notes as we can.
There's a lot of research here,and you can find out all of the
other podcasts, of course, onthe Designs for Health website.
Thanks so much for joining us.
I'm Andrew Whitfield-Cook.
This is Wellness by Designs.
Music.
This is Wellness by Designs,and I'm your host, andrew
Whitfield-Cook.
This is Wellness by Designs andI'm your host, andrew
Whitfield-Cook.
Joining us today is Dr BradMcEwan, a PhD naturopath and
(00:30):
nutritionist who works with theComplementary Medicines Group,
and today we'll be discussingall about vitamin K, mk7.
Welcome to Wellness by Designs,brad.
How are you?
Speaker 2 (00:43):
I'm very well.
Thank you very much for theintroduction.
How are you?
Speaker 1 (00:46):
I'm great mate.
Very good Now.
First of all, we need todifferentiate between the
vitamin Ks, because it's one ofthose much misunderstood
molecules, particularly inmedical circles, who still don't
realise that there's more thanjust vitamin K.
So can you take us through thedifferent side chains, the
(01:08):
different molecules?
What is vitamin K and what isvitamin K2?
Speaker 2 (01:14):
So, first off, I'd like to start by saying I'm very
excited about doing thispodcast and I believe that you
know everyone should have havesome.
Everyone should have somevitamin k2.
And, to finish off with that,thank you very much for all your
attention.
Sorry, just a side joke.
So the exciting thing aboutexciting thing about vitamin k2,
(01:36):
as what you're saying, andrew,is, it's a very wide field of
information and if you think ofit in a way as, yes, there's
vitamin K1, vitamin K2, but whyshould everyone be having some
and what is so special about it?
And one of the areas I want youto think about is let's start
back at the beginning looking atstructure, function,
biochemistry.
Put that in your mind as we gothrough today's journey I'm
(01:59):
going to say today's a journeythrough vitamin K2, because
we're going to cover a widerange of different areas.
So, as we go through, think ofstructure, function,
biochemistry and what's linkingall these things together,
because if you understand that,you'll have a better
understanding of, you know,health and nutrition and sort of
naturopathic medicine ingeneral.
So when we start thinking about, you know, vitamin K, vitamin
(02:22):
K2, cetera.
What is it?
So the two main ones we look atis vitamin K1 and vitamin K2,
named normally in numericalorder, as, like the B vitamins,
it sort of goes in order of whenthey're found.
So one thing I want you tothink about is vitamin K1 has a
vital side chain, so it's sortof like a lipophilic side
(02:43):
structure and that's its maindifferentiating point, while
vitamin K2 has more like acarbon chain, carbon bonding
type of effect, where we'relooking at sort of these repeat
molecules, and that's the maindifference structurally between
the two.
I know it sounds sort of simpleOne's more of a lipophilic and
one is more of a sort ofcarbon-based structure.
(03:05):
But that actually helps benefitthe differentiator.
Two of how they work.
And we always see things likeyou know what is the difference
between minoquinone 4,minoquinone 7, minoquinone 10?
There's all the way from sortof number 2 to number 14.
And that's all based on thenumber of side chains.
So there's your biochemistry.
(03:25):
Very easily, it's just a simplething.
As in, how many side chainsdoes this have?
And in this case, menaquinone 7,which is the focus of what
we're talking about today, has 7.
So I want you to think sort ofyou know, how do we get this?
Where does it come from?
So vitamin K2, particularlymetaquinone 7, is formed in the
(03:46):
gut.
It's formed in our bacteria, sowe can actually manufacture
part of it ourself and infermented foods, of course, from
the bacteria of the fermentedfoods.
So that sort of takes us backto you know, it all happens in
the gut effect.
You know how we talk a lotabout naturopathic medicine is a
lot of symptoms and systems, Ishould say, work from the gut
(04:06):
out, inside out.
So if we keep that in mind,that's a very big area.
If we have good digestivehealth, we'll have better
digestive health related to ourvitamin K2 metabolism,
particularly in Medicare 7.
So I want you to start thinkingabout comparing the pair if you
think about this.
So Medicare 7iQ7 is, we'relooking at, absorbed in the
(04:28):
large intestine, while vitaminK1, phylloquinone is actually
absorbed into the smallintestine.
So it's sort of like the smalldifferences.
To start with, and as we gothrough the different processes,
vitamin K1 and vitamin K2 areboth sort of absorbed and
utilized into our chylomicrons,into our ldl cholesterol as well
(04:49):
.
So we always tend to think ofldl cholesterol as being, you
know, the bad guy causes allthese problems.
But I try and think, hang on,ldl actually does play a role on
the body.
It's very useful for, um youknowuble vitamin carrying, such
as K2, but also other nutrientsas well, throughout the body, so
it actually has a wider role.
(05:11):
So if you think about this,vitamin K2 and K1 gets absorbed
in our gut, gets attached andenveloped, I suppose, by the
chylomicrons and depositedthroughout the body, and
particularly with K1, it goesinto the body, gets picked up by
the VLDLs and gets taken backto the liver where it tends to,
let's say, live its life.
(05:32):
Vitamin K1 particularly does alot of functions in the liver.
The difference with vitamin K2is it tends to utilize the LDLs
a lot more easily and transportto what we call the extra
hepatic tissues that are outsidethe liver.
So vitamin K1 stays inside theliver.
Essentially, after absorption,vitamin K2 goes throughout the
(05:53):
body, and that's what makes itdifferent as part of our
clinical side that we'll talkabout later.
The other thing that's excitingabout vitamin K2 is it crosses
the blood-brain barrier.
So that's something we canstart thinking about later on
when I talk about plaque formingand crystal forming conditions
think of alzheimer's or multiplesclerosis, etc.
(06:13):
That it can actually havegreater benefit in.
So everyone always thinks withk2 is blood and bones, which is
good good to think that way, butwhat we'll be talking about in
this podcast is, you know, alittle bit more than that yeah,
okay.
Speaker 1 (06:30):
So a couple of questions straight off the bat.
If we're talking about in uhmk7 being incorporated into the
ldl molecule, does it have anyprotective effects there, like,
for instance, ubiquinol does,protecting the LDL particle
against oxidation and thereforefoam cell production?
(06:51):
Do we have any evidence thatMK7 has that sort of protection
against atherogenic molecules?
Speaker 2 (07:00):
It's an area I haven't looked into yet but it's
quite exciting because I likethe ability of how vitamin K2
does have that antioxidanteffect and cell protective
effect.
And if you were to combine itwith ubiquinol, tocotrienols,
for example, and other similarantioxidant molecules, you could
predict from small, dense LDLslike the golf ball effect of it
(07:22):
smashing into the arterial walls.
Like the golf ball effect of itsmashing into the arterial
walls.
So from my thinking of goingback to, like I mentioned
earlier, our structure functionbiochemistry, short answer is
yes, I think from what weunderstand, it will do that.
It's not an area I've lookedinto but I will now.
But it's something that I thinkwill actually make a big
difference of our understandingof how vitamin K2 does that work
(07:44):
.
Speaker 1 (07:45):
Yeah, and another one .
Sorry, brad, to go straight offthe bat, because you piqued my
interest, and that was whenwe're talking about being
incorporated or helping theliver.
Do we have any evidence yetthat vitamin K2 MK7 might be
(08:09):
beneficial in conditions,metabolic conditions like, um
well, we used to call itnon-alcoholic fatty liver
disease, but we realized thatthere was too many people
drinking not having none, um, soI think the acronym is now
massaled.
Is that right m something?
Speaker 2 (08:21):
like that.
Yeah, there's a lot ofmetabolic associated.
Speaker 1 (08:25):
Metabolic associated don't know what the host in
their liver disease muscle.
Um yeah, I think the acronymschange, but do we have any
evidence yet that MK7 is abenefit in those conditions?
Speaker 2 (08:40):
not that I've seen particularly like related to
what you're saying, but if youlook at the wider aspect of how
non-alcoholic fatty liverdisease or fatty liver disease,
cirrhosis or any of these liverdiseases work, the short answer
again is yes, I believe it willactually have great benefit in
that area because it is workingthrough the regulation of
(09:01):
cholesterol metabolism,antioxidant, anti-inflammatory
pathways, calcification pathways, which I'm about to talk about.
So I do think that we are goingto see more benefit in that
research.
The main sort of focus ofresearch of K2 that we'll be
covering has been extrahepatic.
They haven't really beenlooking at the liver.
But if you think of thevascular system, of course the
(09:25):
liver is very highly containedof vascular tissue, so that's
how part of the filtration unitaffects.
So with my understanding of howit works, it would definitely
greatly benefit.
And there is research withtocotrienols, for example, of
reducing the impact ofnon-alcoholic fatty liver
disease or fatty liver disease,adiposity-based conditions,
(09:47):
which is where there's a newcondition-based ABCD they call
it, which is sort of adipose B,because I can't remember,
because I just thought of itcardiovascular disease, like
they've tried to do like analphabet kind of thing where
each letter means something andit may have an adipose based.
It may be as simple as that.
Um, yeah, right, but it's whereyou start thinking about.
(10:10):
You know, when we do haveadipose tissue, whether it's in
the gut or the liver or aroundthe heart or brain or any other
area, you know it's on fire andit's causing some inflammatory
effects and if you think of anyway that can greatly benefit the
blood flow.
The antioxidant,anti-inflammatory capacity which
vitamin K2 is working in thebackground of, I think it would
(10:32):
greatly benefit in thosesituations.
Speaker 1 (10:35):
Yeah, Okay, so K2, then we've got the different
molecule lengths.
We don't have it here, as is myunderstanding in Australia, the
MK4.
The one that we have availableis MK7, but the molecule lengths
go right up to what?
13 or something.
(10:55):
Is that right?
Speaker 2 (10:56):
So 13 and recently 14 .
So we're finding, you know, alot more research as we go
through, and that's the benefitof you know where we're going
with nutritional medicine andnaturopathic medicine in general
.
So it's not just science.
You know research, of course,but it's how we apply it and
that's where, in the year thatwe're in, it's very exciting to
(11:18):
see a lot more research comethrough.
And there is some MK4 researchout there, so metaquinone 4.
They tend to call it MK, sometaquinone, k2, and then they
break it down into its numbersMK7 is metaquinone 7, metaq7.
So if you think about it, thelower the number, the shorter
the molecule, the longer thenumber.
(11:40):
You know the long chain kind ofeffect.
So if you keep that in mind,that seems to be the way how it
works in the body where the longchain kind of effect.
So if you keep that in mind,that seems to be the way how it
works in the body, where thelonger numbers seem to be more
flexible.
So particularly mk7,metaquinone 7, being in that
mid-range, it is classified as along chain vitamin k.
So I want you to start thinkingabout long chain fatty acids
etc.
It's the same kind of thingwith k2, is you've got different
(12:03):
lengths doing different thingsand a lot of the research is
still based on this sort ofmenoquinone 7 effect because
they're finding that's where ithas the greater effect, because
it seems to have that sort ofmore bio flexibility of the
molecule compared to the longerchain and the shorter chain and
being in the middle it seems tohave that greater effect even
though, as I said, it's stillclassified as a, as a long chain
(12:25):
.
And what I'm thinking about is,as we go through this podcast
and general conversations is, um, there's always new ideas
coming up, like the more wethink about with you know,
biochemistry, and it's a verygood question, you know, with
the length of the structure andhow it works in the body.
Um, again, thinking oftocotrienols with the bifatal
structure and how it works inthe body.
(12:45):
Um, again, thinking oftocotrienols with the biphatal
tail, it's able to move its wayinto the fatty tissue, into the
cell membrane, work antioxidantinside and outside,
anti-inflammatory inside outside, outside in.
So it sort of goes both ways.
We're finding that a lot morewith vitamin k2 now is it's I'll
use the word biphasic, whereit's able to sell signal inside
(13:06):
out and outside in toincorporate a lot of these
changes.
It's quite exciting right?
Speaker 1 (13:12):
yeah, absolutely.
If we're thinking about foodsources, though, like I have not
looked into this at all withregards to chain length, all I'm
aware of is things like nattohence natto farmer, but from the
natto beans with what is abacillus subtilis fermentation.
(13:34):
And then there's cheeses, aswell Swiss cheeses.
I don't know of any othersource and I don't know about if
either, or which foods are morelinked with different side
chains.
Do we have any knowledge ofthat?
Like you said, like we've nowelucidated, a side chain of 14,
(13:58):
so an MK14.
Do we know what foods that'sfrom?
Or is that only from, like,fermentation of bacteria in the
gut?
Speaker 2 (14:06):
Seems to me more from fermentation in the gut, but
also they're finding it in somefermented foods.
So, going back to the natto,which is a fermented food, I'm
thinking, you know, let's jumpahead or back in this case,
things such as, you know,sauerkraut and other just
general fermented foods thathave been around a long period
of time.
We've always used them fordigestive health for centuries
(14:28):
and not really knew how theyworked, and we're still finding
out more and more details aboutfermented foods.
So it makes me think, you know,vitamin K1 is mainly found in
green leafies, for example.
That's one of the main sourcesof it, as we were working on
earlier, and K2 is more infermented foods.
So I'm going to suggest anymajor fermented food with that
(14:52):
sort of bacillus that we werejust talking about.
That seems to be where it'sfound and again in our gut.
So we've got a whole ecologyworking with us or against us in
some cases, that could beworking with metabolising.
Speaker 1 (15:06):
Yeah, okay, so the uses, if we go into, I think the
initial work was done on bones,but then it took a side thing
and was looking atcardiovascular disease.
There was other potential usesas well, depending on the.
What is it the proteins they'reworking on?
Is that right?
Speaker 2 (15:26):
That's right.
So there's a number ofdifferent areas.
So what I was thinking ofbecause when we were originally
talking about this, I wasthinking how can we go about,
you know, discussing thebenefits of vitamin K2 in a
short amount of time, because wecould talk all week about this,
and I was thinking let's gothrough some base health
(15:47):
conditions first and then sortof you know, expand on those.
So the main functions or uses,of course, is improving bone
health.
That's one of the main areasthat they looked at.
You know, reducing fracturerisk there's a lot of research
on that.
Vitamin K2s Everyone alwaysthinks of, you know, calcium and
vitamin D.
That's great because that doeshave a lot of evidence in
(16:07):
phosphorus or phosphates for thebone structure matrix.
But you also need something tosort of direct and work things
out, as in I see vitamin K2 as adirector in a lot of these
areas.
So whether it's blood, bone,other tissue we're about to talk
about and that's what I likeand find exciting about vitamin
(16:28):
K2 is that it is like thedirector.
So we've got other areas suchas blood coagulation, which is
well known.
We keep looking back into that.
Just overall, cardiovascularhealth reducing cardiovascular
risk and mortality, reducingvascular calcification, which
we're going to be talking aboutshortly, reducing arterial sort
(16:48):
of stiffness.
So I want you to imagine thecardiovascular system is like a
hollow tube, as we know, and ifthe hollow tube is flexible and
flowing properly, we have goodblood flow.
Once it becomes sort of stiffand sort of more restricted,
that's when you get yourhypertension's and your
hemorrhages and your vasculardepletion, strokes, heart
(17:09):
attacks, dvt, etc.
Um, metabolic syndrome.
There's a lot more researchthere where vitamin k2 is
working hand in hand withinsulin, which is pretty cool.
So, remember, we're moving awayfrom the original side.
Now, improving chronic kidneydisease, which could also be
related to, you know, type 2diabetes, vascular, yeah, wide
(17:31):
range of different healthconditions.
Of course, with chronic kidneydisease, kidneys are very tough.
You don't normally noticethere's a problem until there's
a big, big problem and, yeah,they don't feel pain too much.
So therefore, they have to bereally large or really small and
sort of I'll use the worddamaged for them to actually
tell you that there's a problemwith themselves.
(17:51):
They're quite tough.
And also just reducingage-related chronic disease
states.
We're finding out.
So, you know, in the lastdecade or so there's been a very
big push for vitamin d3 and youknow vitamin d3 markers and
having x amount of um in theblood, for example, when you do
a blood test should we be alsomeasuring for vitamin k2,
(18:11):
because they work in a similarpattern of chronic disease
prevention or risk reduction?
So I was thinking, sort oftaking us on a bit of a journey
through vitamin k2, if you like,about how it works.
I like stories when it comes tothis because it helps me
remember how it works.
So I want you to start thinkingabout.
(18:32):
You know, vitamin k2 is amultifunctional molecule,
multifunctional nutrient vitamin.
So yes, it starts with thebones that's where we know but
actually starts working in a lotof wide range areas as well.
So it works with a lot of enzymepathways.
So one of them's and I'vewritten down some notes, I
remember how to say them rightgamma glutamyl carboxylase
(18:55):
enzyme pathway, which sort ofworks with glutglutamyl
carboxylase enzyme pathway,which sort of works with
glutamic acid.
So carboxylase is glutamic acid.
So COOH bonds, et cetera.
It seems to work withfunctionality there.
It works with I love this namevitamin K dependent proteins.
I'm like whoever thought ofthat name one day was on fire.
(19:16):
It's like naming Sydney Harbour, sydney Hardney harbour bridge
and sydney opera house andsydney cove.
Like those people get paid bigmoney um great sandy desert
great sandy desert, let's getgum.
Um.
Western australia, northernterritory, south australia.
You did really well.
So.
So this day this person was onfire and called them vitamin k
(19:37):
dependent proteins.
So that really works for me.
So it says what it is.
So one of these particularproteins that works with the I'm
going to call it theglutamization new word of the
day doesn't exist.
Glutamization is osteocalcin.
So we do know osteocalcin.
So if you, whenever you'retrying to understand a word that
(19:58):
you've never heard of and thisis for a lot of our viewers who
may be starting off in theircareers break it down
Osteocalcin, osteo normallymeaning bone calcin, calcium, so
transportation of calcium, andit's synthesized by the
osteoblasts.
The osteoblasts, of course, arebone cells that form and create
(20:19):
things.
This is forming duringmineralization phase of the bone
.
So osteocalcin is veryimportant for bone health and it
binds to the calcium ions andthe hydroxyapatite crystals,
regulating size and shape.
So I want you to imaginebecause we're going to stick
with the bones and start withthe bone matrix One of the main
stages of working on bone matrixis between the ages of eight
(20:41):
and 10.
So, andrew, you and I are alittle bit gone past that point
of ages eight and 10, but we canstill keep working on the
regulation of that because upuntil about the age of 21 to 25,
which is the category that youand I are in it seems to be
still forming and working to getthat sort of solidification for
(21:02):
the rest of our life.
But what I want you to rememberis we're always building,
breaking down.
Nothing is ever set in stone,so to say, because red blood
cell is 120 days, like platelets7 to 14 days, like things are
always growing and developing.
We're growing and developingfrom the moment we're conceived,
(21:24):
the conception of who we are,all the way to the end.
We're always growing anddeveloping in all different
areas.
Everyone always seems mentallyand physically, for example, and
emotionally growing.
But physically the body and thebiochemistry is always growing
and developing.
So our bone is always in thisconstant state of flux, where
it's always moving and it'sregulating and it's changing.
(21:46):
So if you sit down and donothing all day, your bone
mineral density will change,probably go to your buttocks,
because you're sitting on it allday doing nothing.
But if you get up and becomeactive and that's the comment I
made about ages of 8 to 10, upto 11, because you're physically
active and you're actuallyimpacting and pounding on that
(22:06):
bone, and gymnastics and tennisand a lot of these force
activities create that bonestrength.
Swimming doesn't, of course,because it's not weight-bearing
those kind of activities, butanything that's moving,
including just walking, startsthat process.
Swimming doesn't, of course,because it's not weight bearing
those kind of activities, butanything that's moving,
including just walking, startsthat process.
So getting up and moving, andthat's when we start to develop
and those crystals then start toform and our bone starts to
(22:27):
form shape to where it needs tobe.
So, whether it's a long bone ora finger bone or anything else
like that, again, it's the oldif you don't use it, you lose it
kind of mantra that we say witha lot of things.
So if we keep working with thisosteocalcin and this is where
we start to visualize in ourmind that it's sort of creating
(22:47):
a higher affinity to thishydroxyapatite mineral bone
content and it's actuallydriving in calcium and other
nutrients, of course, into thebone tissue and that's what we
really want.
So I want you to start thinking.
This is like a link betweengeochemistry and biochemistry
now.
So I want you to start thinking, because you know geochemistry
(23:09):
is all crystal formation,minerals, et cetera.
So in some cases some peopleare just big walking crystals.
You know, I want you to thinkabout that.
So they've got the bone mineraldensity that's changing.
They may have gout, which iscrystals as well.
So there's a lot of areas thatsort of start thinking about
crystal formation and it's goingto the wrong place.
(23:30):
And osteocalcin, being driven byvitamin K2 and of course
vitamin D3, is working on thisjourney.
So again, we're sort of workingwith visualisation of bone
forming and other tissueutilising it and if we think of
that process we can startthinking about what else happens
.
So osteocalcin then startsworking with energy metabolism,
(23:53):
bone metabolism, endocrinefunction.
So all the different endocrineorgans are starting to become
involved.
So this is all part of ourmetabolic health, because our
bones are metabolic, our bloodis metabolic.
So if you think aboutregulating energy metabolism and
just overall health, that wayit starts working.
And another role which we'lltalk about later is it has this
(24:16):
inhibitory role on angiogenesis.
So angiogenesis, of course, isthe formation of new blood
vessels and we want that tohappen for general health, but
we don't want that to happen incancer, because the generation
of new blood vessels means bloodflow for the cancer cells,
which means growth anddevelopment of them, leading to
cancer formation.
(24:37):
As a brief storyline, it alsoregulates ectopic tissue
calcification.
So ectopic always means awayfrom sort of where it should be.
So in this case we're talkingabout blood vessels.
So there's a wide range ofdifferent areas that we're
working of, just with theosteocalcin side, and it's a
transporter, and we're journe,just with the osteocalcin side
and it's a transporter, andwe're journeying through the
(24:58):
body, and that's what I like.
Start to thinking about allthese vitamins and minerals and
amino acids and everything goingon a journey for our for our
nutritional needs.
Yeah, there's another protein.
There's the matrix GLA proteinthat keeps working with this and
that works with thecardiovascular disease health um
.
Speaker 1 (25:16):
So the matrix GLA proteins.
Brad, can you tell us moreabout those, what they do so?
Speaker 2 (25:22):
again I want you to think about.
You know the terminology matrix, GLA.
So we always talk about thematrix, not the movie, but the
actual matrix in the body, whereit actually works by.
It's like a netting, astructure.
It's hard to explain sometimeswithout using too many hand
motions Cellular matrix, tissuematrix, organ matrix.
(25:45):
It seems to work by, you know,piecing and putting things
together into its cell structure, into its system, and that's
what I find interesting, wherethere's this communication
between cells that are the samecell but also other cells.
The body has this amazingcommunication with itself.
It's just and again, in today'syear we're still finding out
(26:08):
the way, how.
You know, I'm fascinated by howthings work, how we can talk
and think and walk and text anddo all the things all at the
same time.
And it's the body's, you knowmatrix system itself working and
communicating with each other.
And this gla matrix is one ofthose areas and what I was
thinking about, as I mentionedearlier, sort of going through a
(26:29):
bit of a journey into um.
You know, applications of, ofhow we could utilise, you know,
menaquinone 7, K2, and you'vegot to say it's low.
Speaker 1 (26:42):
So the evidence we started off with earlier work by
Thuisson and his group.
What is the evidence nowshowing us?
Because there was some positive, some negative evidence, but
when I looked further it waskind of like what was one of
(27:02):
them there was a positive changein the lumbar vertebrae but a
negative change in the.
Was it radius, radial density,radial bone density?
So it's almost like what youwere talking about earlier about
(27:23):
that need for exercise.
Now I don't know about this.
It was just an interestingthing.
Tell us more about the researchand where it's leading us.
Speaker 2 (27:35):
And that's the exciting thing.
There's a lot of interestingthings that we can really move
into as we go through and I wantyou to think back.
Most people now are becomingmore sedentary over the last few
decades.
We're working more inside, lessactive.
I have my Apple Watch, where Ideliberately have it set, where
I have to get up regularly andmove around so that keeps
(27:58):
circulation going, keep the bodygoing metabolic-wise, and
that's what I'm thinking back to, that study that you're
mentioning, that the lumbarregion is being used more
because you're sitting on it,for example, and you're using it
more as weight-bearing.
While your wrists may be on thedesk, they're not really working
as much.
You may be typing or using themouse, but it's not weight
(28:19):
bearing as compared to yourlumbar.
But if you start exercisingmore and actually moving moving
and grooving and moving around,you start to use that.
That's where some people useweights, you know, like the
wrist weights or just do that.
That's weight bearing still, umyep, so holding it using a
mouse is not weight bearing, butit's sort of like any kind of
(28:39):
activity.
So you know, if you need to getup from your desk and do like
the old 1980s sort of aerobicexercise around the office where
you're punching the air andmoving around, because that sort
of gets things up and movingand then you can add some weight
bearing to that.
Um, so what I'm thinking if Igo through some of the research
(29:01):
that this is leading to, andthen we can have a good
discussion at the end, becauseit's sort of quite exciting
where, where we're going, andpart of that is, of course, you
know, cardiovascular disease.
We're looking a lot morevitamin k2 and quinone 7,
cardiovascular disease.
So one of the areas I mentionedearlier is coronary artery
calcification.
So what is it?
(29:22):
The name it says we're verywell named.
Coronary artery is calcified.
There's a calcification processhappening and it's a very
significant predictor ofcardiovascular disease and
cardiovascular disease risk.
And there's some pioneeringwork in that area where you can
look at calcium scores et cetera.
So one of the areas we've beenlooking at is a deficiency of
(29:44):
vitamin K2 has been linked tovascular calcification, not just
coronary but just overallvascular calcification.
And if you think of it this way,you've got different mineral
deposition, particularly calciumof course, coming from the
calcium hydroxyapatite and wealways say from the bones,
because that's the main storagesite into the vascular system
(30:05):
and then going into the vascularwall because it gets trapped.
So it's like a big centrifugalforce going through the arteries
and then it just gets trappedbecause it's I don't know
heavier.
It's like a big metal goingthrough and it embeds in the
overtime.
As you know, we're talkingabout foam cells,
atherosclerosis etc.
And it starts that calcium youknow process and this deposition
(30:27):
also combines phosphates, otherminerals I'm going to suggest
even heavy metals get involved.
Um, I had a patient many, manyyears ago that had an issue
where no one could work out whatit was and we ended up working
out.
Long story short, the GP camein with her and it was a very
serious case and her files werecan't see my hands, but really
(30:50):
massively printed out, everytest under the sun and I just
about you know bone deposition.
Everything that we sort ofmentioned today and what I found
out was due to her childhood.
There was different heavymetals in the area and that's
what deposited into the tissueand when she moved around, that
tissue left because she didn'thave enough vitamin d, vitamin k
(31:11):
etc.
And then left the bone.
So she had bone pain and thenembedded into her vascular
system, leading tocardiovascular risk.
So that was a good example ofsomeone that had heavy metals as
well and metals combined withmetals.
If we go back to our anions andcations and everything else
like that, they all thebiochemistry all combines
(31:32):
together, leading to thiscomplex which then sat in the
arteries and it can sit in thebasement membrane of the artery,
it can be on the inner or outerside of that membrane, leading
to an inflammatory process, anoxidative process, leading to
like a firestorm in there.
The body tries to heal it bylaying down, you know, fibrin
(31:53):
and different connective tissueto help protect it, putting a
Band-aid down, I suppose.
And then that's when you getyour atherosclerosis, your
plaque formation and then, yeah,your eventual clot in that area
yeah, yeah so it's.
It's a big process.
So if we think about that asoccurring and then we reverse
that process by thinking, okay,we've covered today, thinking
(32:16):
about vitamin K2 and how vitaminK2 works with osteocalcin
crystal deposition, you know themicrocrystalline fibers in the
body, and then you've got yourcell matrix and hydroxyapatite,
we can then start moving anddirecting, as I said, vitamin K2
to me as a director, directingit to the right place.
(32:36):
And it sounds very sort ofstory-like, but that's the way
how a lot of our body works.
It's a big story that's beendirected by our DNA.
The main director, like ourgenetic code, is telling
everything what to do.
So if you think about, you knowthat different process, just
with this calcium, you knowfortification in the coronary
(32:59):
artery and other areas, we canstart thinking about vitamin K2
and how that can benefit.
And there's a lot of differentresearch studies coming out of
you know the really longitudinalstudies.
So these studies have beengoing on, you know, like the
Framingham Heart Study, the LeonStudy, the Nurses Study, the
Health Practitioner Study, theStates Nurses.
(33:21):
There's a lot of researchstudies now where they can look
back over test results from thepast.
There's blood samples from the1940s and 50s and stuff that
they can actually pull out ofminus 80 freezers and actually
test it for new inflammatorymediators that were never around
even 10 years ago.
So they're able to do a lotmore of this research.
And a lot of research isstarting to show not with just
(33:44):
those kinds of studies but otherstudies that vitamin K2
depletion over a period of timehas led to a higher risk of
arterial calcification as wellas just general calcification of
the body in the wrong areas.
Speaker 1 (33:59):
Yeah, this is one of the areas that interests me in
that when looking at theresearch, some of this negative
research was coming out sayingthat vitamin K2, mk7 did not
reduce coronary artery calciumscore.
But I know, clinically it damnwell does.
I had an elderly gentleman whohad a I mean, you'll fall off
(34:24):
your chair when you hear thiscoronary artery calcium score, a
CAC.
The CAC was originallysomething like 5,000.
Now I haven't got the thingsdirectly in front of me, but it
was something in that vicinity,whereas anything over 400 is of
clinical like Huge clinicalsignificance 15% risk.
(34:46):
So this was in the thousands.
Upon taking now I'd have towork out the exact dosage.
Forgive me, but on takingaround about five, six, so let's
say 300, forgive me, forgive me600 micrograms of k2 combined
(35:13):
with 6 000 of vitamin d, plusthere were some other
supplements in there.
Because of the healthconditions of this gentleman, um
, within a six month period, hiscoronary artery calcium score
was reduced by half.
Now that's still massive.
It's still massive.
Speaker 2 (35:35):
It's still 2,500, but that is a significant reduction
in risk.
So this person was leachingbone.
Speaker 1 (35:40):
There was a ticking time bomb, and you're right.
You're right leaching bone.
So it makes me query thequote-unquote evidence where
they say no, it didn't, whenI've seen it work like that.
It definitely does reduce CAC.
Speaker 2 (36:00):
It definitely does.
And dose we'll talk about laterbecause I've got a couple of
points I want to make.
On dose, you know veryspecifically for what you've led
into it very well actually, um,where I'll talk about a couple
of clinical cases as well.
So what I'll do, I'll finishoff this journey and then I'll
(36:20):
talk about the reasons why Ibelieve that those doses do work
in some cases and don't work inothers, because it's sort of,
once we have an understanding ofyou know where this journey is
going, you'll see why certaindoses work, and that goes with
any nutrient, any herb, ofcourse.
So if we continue through ourturbulent journey of our
(36:43):
vascular system forging ahead,you've got arterial stiffness as
well.
So you've got the calcification, you've got the stiffness.
Now, thinking about that personyou just mentioned, they're
turning the stone with thatcalcium score.
It's a very high calcium score,so they're literally turning
the stone.
So arterial stiffness as wellas vascular calcification are
(37:06):
very good predictors ofcardiovascular and overall
health.
I'm going to say so.
A lot of test results can letus know overall health.
So there was a NAPN study whichis quite well known.
There was a double-blind,placebo-controlled, and I've got
to get the number right, I'vegot it in front 244 healthy
postmenopausal women, becauseyou've always got to throw in
(37:26):
the healthy part.
So healthy typically means thatthey don't have the condition
that they are testing for.
So in this case it was 244healthy postmenopausal women.
They investigated the effect ofvitamin K2 at 180 micrograms a
day, which is a standard dosethat we use in Australia.
120 in that and placebo is 124people for three years.
(37:51):
So having any nutritional studyfor a month is pretty good.
Six months is really good.
Three years is really reallygood.
So the longer the researchstudies the better.
So after three years they foundthat K2 improved arterial
stiffness, so the artery is moreflexible.
So sometimes we have to becareful when we say improved,
(38:14):
because the word can go bothways.
So improved arterial stiffness,especially in those with
already high arterial stiffness.
So it sounds quite interestingthat in the people that already
had a high level of arterialstiffness they had a very good
improvement in their blood flowand a reduction in arterial
stiffness at that dosage of 180,versus what you were mentioning
(38:38):
earlier.
They seem to have also had areduction in the GLA protein
matrix area that was seen to behaving a negative impact.
So the flow of calcium in thebody was seen to be more
improved.
So that's just one study.
There are quite many more wecould talk about but due to time
(38:59):
I'm trying to have greaterexamples of each one.
If we go from arterial stiffnessto a wider range health
condition, now called peripheralartery disease or arterial
disease.
So we've gone fromcalcification to arterial
stiffness.
Now we're looking into adisease state name, I suppose,
(39:20):
and this is our journey.
So peripheral arterial diseaseor artery disease is actually
more common than you think.
Arterial disease or arterydisease is actually more common
than you think.
So think of the name peripheral.
So legs, arms, hands, feet, youknow arterial, just arterial
blood flow in disease is justdisease, it's just a condition.
Base Now what they've realisedand worked out with research,
(39:45):
again with longitudinal studies,that a low vitamin K2 status
has been associated withincreased risk of peripheral
arterial disease.
So again, they've been lookingat a lot of studies.
So here's a little study foryou, andrew, sorry about that A
12-year study.
So here we go, 12 years onvitamin K2.
(40:06):
So this was the intake,measuring the intake on a small
number of people, 36,629.
So here we go.
This is where we want the gutsof things now.
So this is where we really seesome really good research come
through.
At the end of 12 years, vitaminK2 intake was associated with a
(40:30):
reduced risk of peripheralarterial disease, with a hazard
ratio of 0.71.
So what this means for theaudience is hazard ratios are
quite interesting to look at.
If you think about it, if youhave a hazard ratio of 1, you're
likely to get it it.
If you have a hazard ratio ofone, you're likely to get it.
If you have a hazard ratio of1.5, you are 50 percent more
(40:53):
likely to get it.
In this case we are 0.71,meaning there's a 29 because you
take that from one, 29 lesschance of this happening.
So that's the hazard ratio.
So I think that's a pretty goodnumber that you know.
Your vitamin K2 status overthat period of time meant you
had a 29% less you know chanceof this happening.
(41:15):
10% for me is great, if youknow what I mean.
Statistically, of course, thehigher or in this case, the
lower the hazard ratio, thebetter.
High blood pressure was measuredin this study as well, because
I measured a lot of differentareas.
Hazard ratio was 59, sorry,0.59.
So there wasa 41.
(41:36):
Reduction in risk.
Type 2 diabetes had a hazardratio of 0.56.
So we're looking at a 44%reduction.
So this is just from the humbleintake being measured of
vitamin K2.
So I think it's quite excitingto see a lot of this base
research being done.
(41:57):
Of course, it's large numberswhen we get this.
But something very interestingfor me, going back to where we
first started, the intake ofvitamin K1 had no association
with reduction of peripheralarterial disease.
Right, and why is that?
Think back to when we firststarted.
Speaker 1 (42:19):
It's different molecule length, but yeah.
Different molecule length, Imean, but not just molecule
length.
There's an answer.
It brings into question thingslike methylation as well.
That's it On treating anexisting condition.
Speaker 2 (42:37):
So the winner of this gets a copy of my book to be
published.
So this is a question for theaudience.
You get a prize, but I'll giveyou the answer as well.
So at the beginning, vitamin K1I mentioned is intrahepatic.
It mainly stays inside theliver.
Vitamin K2 is extrahepatic,meaning it goes out to the
(42:58):
tissue.
So vitamin K1, for example, inthese patients, stayed within
the biliary, stayed within theliver system.
So therefore it would generallynot have an impact on
peripheral arterial diseasebecause it's in the periphery,
while vitamin k2 floats we'lluse the word floats floats
around the body on our ldls andchylomicrons and everything else
(43:19):
like that.
So therefore it's able toachieve its point.
So there's a good example ofwhere k2, being extra hepatic,
is able to do something at thefar ends of the earth, being the
hands, feet, legs and arms.
So goes back to, like Imentioned earlier, structure,
function, biochemistry.
Every time we need an answerthink back.
(43:40):
The answer may not bescientifically proven yet, but
we start to think back in.
What are we thinking about?
It's the physiology, thebackground work.
In this case, that's my answeris k2 did the job because it's
extra hepatic, it went outsidethe liver and did its job rather
than inside the liver.
They didn't do any hepaticmarkers, which would have been
(44:00):
interesting to see, of course,but that's another study to be
done.
I could yeah, well, andrew,both of us could sit down and
write a whole heap of studiesabout what we'd like to research
right now.
It's quite exciting.
Speaker 1 (44:15):
Brad, we spoke earlier about doses.
We need to cover this off.
What doses are appropriate?
Can I quickly ask, by the way,that large study that you were
talking about before, was thatthe Rotterdam study, or was that
a different one?
Speaker 2 (44:30):
It was a different one and I can't remember the
name right now, but it was adifferent one.
No, that's all right.
Speaker 1 (44:34):
They all have different acronyms.
That's fine, can we?
Cover off on dosages, becauseone of the things that's
interesting me is out ofconvenience, we tend to combine
D3 and K2.
Is out of convenience, we tendto combine D3 and K2.
But the more I learn about K2,the more I'm wondering about the
(44:58):
formulae on the market.
Are we wasting the K2?
Are we taking not too much,necessarily, but are we just
wasting the dose?
Should we indeed be taking D3separate from K2?
Speaker 2 (45:07):
That's a very good clinical point when I was
thinking about talking with youabout this.
Is you know how far do we go?
Because I've got notes in mybrain on metabolic syndrome,
peripheral neuropathy,alzheimer's disease, multiple
sclerosis.
There's a whole heap ofdifferent avenues we can go down
(45:28):
to Some of these studies.
Are you know, I'm just thinkingof one now 625 people over 10
years for metabolic syndrome,type 2 diabetes.
There's, you know, a lot ofdifferent avenues and some of
this sometimes comes down toactual dose.
So think about the applicationsports gout, other health
conditions.
It comes down to actual dose.
So think about the applicationsports gout, other health
(45:49):
conditions.
It comes down to dose.
Now, typically the doses we usehere in Australia we are
limited with TGA, so therapeuticgoods administration on doses
of vitamin K2.
So appropriate doses, I'd say,is based on the age group.
So typically adults are 90 to180 micrograms per day.
Based on the research like theNAPN study and a lot of other
(46:12):
research is based on that dosage.
900 to 180 micrograms, sorry,90, not 900.
90, please.
90 to 180 micrograms per day.
Children 10 to 18, becauseclinically they're seen as
children still up until the ageof 18, that's 90 micrograms per
day.
Children 10 to 18, becauseclinically they're seen as
children still up into the ageof 18.
That's 90 micrograms per dayand children less than 10 years
(46:33):
of age is 45 micrograms per day.
So I'll talk about safetyavenues in a moment, because
that's something that you and Ihave discussed over coffee about
.
You know, safety of um,nutrients and nutritional
medicine, etc.
The reason why I think thedoses can be too high is it
(46:55):
comes down to metabolism.
So it's too much of a goodthing is a lot.
So you know there's an oldsaying someone's what is it?
Someone's doses, someone'shealing and someone's poison.
I forget the whole phrase, butthere's a phrase of.
You know it comes down to thedose of the person and if a lot
of research is being basedaround this 90 to 180 micrograms
(47:16):
in in adults, that's that's anarea that we seem to really need
to sort of focus on and keepingin mind.
Is it making the pathways workmore effectively?
Is it, you know, depositingcalcium crystals more
effectively?
It's, it's hard to say becauseI haven't seen a lot of that
toxicology data, for example.
(47:37):
But you start to think abouthow things work.
Are we wasting it with?
You know, combining k2 and d3?
Um, no good.
No, it depends on the formulaand, of course, the person in
front of us, and that's onething I always want to say when
we do podcasts and everything isit's always the person in front
of you.
What is the best dose for thatperson?
(47:58):
And if they need 500 ius ofvitamin d and 90 micrograms of
k2 from your determination,that's the dosage that they need
.
If they need a higher dose of,you know, 1,000 IUs vitamin D3
and 180 micrograms K2, that'sthe dose regime and that's where
(48:19):
a lot of the evidence isshowing.
So going hard and fast is notalways the best way to do it,
because to me, it's trying topush too much through all the
time.
Um, we get excited.
Some studies are very, very highdose and they seem to have the
negative impact because Ibelieve the regulatory pathways
are not able to functioneffectively to make sure we get
(48:41):
the best out of you.
Know what it is.
A good example is waterDehydration.
Water is very bad for you, butso is drowning.
So if you stick to the 30 milsper kilo body weight per day,
that's the NHMRC guidelines forwater, for example, or fluids,
including tea, coffee and don'tget me started on the caffeine
(49:03):
argument, because when you havea coffee you're having caffeine
with water, so therefore itrepletes at the same time.
Um, if you think of it that waythat's the guidelines based on
the evidence then if you startdrinking five, six, seven, eight
, nine I've seen some people do10 liters of water a day and
they're always feeling sluggishand bloated and feeling bad,
(49:23):
it's over hydration.
You're drowning the cells withfluid, you're going against the
concentration gradient.
Sodium, potassium, pumpnutrients, electrical impulses
are not working effectively andyou can get you know fluid in
the brain and die of a stroke orsomething like.
Let's just go serious for asecond.
That's simple, by changing thedose of water.
Now, if we bring that back to amicrogram molecule such as
(49:47):
vitamin K2, and even D3, it's inmicrograms as well.
As I use, these are based ondoses that the body seems to
accept quite well in metabolicstudies and seems to do the
actions that we need.
And I believe that, like withanything, if we smash the body
hard, these channels that thebody has based on evolution from
(50:10):
when we're cave men and cavewomen and didn't eat every day,
and you stored you knownutrients in the body for a
period of time and used them asneeded, we didn't eat as much as
what we do now.
We have food available 24 hoursa day.
The body's mechanism ofmetabolizing and trying to clear
excess you know toxins but aswell as nutrients is not as
(50:33):
functional as what we're pushingin.
So that's what concerns me whenI see very high doses and some
of these studies are actuallygood for us because then we can
see ethically maybe not, butsome high dose studies, we can
see how well something works.
But also get the differentthresholds, because if the
research showed that you knowcurrently 180 is good, but let's
(50:56):
just double it to 360micrograms is a good dose, we
need to then change ourguidelines in australia to meet
that.
But currently, like I, the NAPNstudy and quite a lot of few
studies out there are actuallyshowing that the dosage between
90 to 180 micrograms to adultsseems to do the work.
Speaker 1 (51:15):
I take your point and you know I was thinking about
the risk of possibly not givingenough credence to other
important signals, likeinflammatory signals, for
instance in cardiovasculardisease and calcification.
Brad, there was one more thingI just wanted to ask you and
(51:38):
that was so maximal dose.
We should be really looking atthat 180 micrograms, maybe a
little bit more, depending onwho's in front of you.
I get it, but not going wayhigh, not going too high because
of those other things.
That's right.
There was one study I looked atand even though it was a high
(52:01):
dose and forgive me, I can'tremember the dose there was no
risk of extra.
Let me word that correctlythere was no extra risk of
thrombosis.
So it wasn't acting like avitamin K antagonist, if you
like.
Speaker 2 (52:18):
And that's something that we discussed recently
ourselves, like talking aboutinteractions with pharmaceutical
medications, for example.
Example, and it does alwayscome down to the person in front
of you.
You know what medications arethey taking, what other vitamins
, minerals are they double,triple dosing on things?
You know what kind of effectare we looking at and there are
(52:41):
a number of um studies that wereout there and one of them
showed there was a small studythat showed 45 micrograms a day
decreased the mean value of INRin.
Some patients say yeah, inr isrelated to blood coagulation.
So if you think of it that way,a lower INR means the blood
clots more rapidly and a longeror higher INR means it takes
(53:05):
longer.
So that was one study andthat's the one that tends to be
picked up by people.
There's always certain studies.
So I always turn around and sayread the studies, read the
research.
You know, understand the personin front of you, look at the
genetics, the biochemistry,physiology, etc.
And always be careful what youread.
Read the full journal article,because the abstracts always
(53:27):
look good until you read thefull study.
I'll give a quick examplebecause I know we're running out
of time.
But there's a big omega-3 studypublished many, many years ago.
That said, omega-3 was reallybad.
It leads to thrombosis andclots and hemorrhages and will
kill you.
And I've gone, wow, I did myphd in omega-3.
So I'm freaking out now going,wow, what's going on?
So I look into it and this wasa case study, so I'm going.
(53:50):
Okay, case studies are good.
It's a level of evidence thatwe need.
It was a man in his 70s okay, sohe wasn't young.
He was admitted to hospitalwith hemorrhaging and further
investigation, which was sort ofwritten in a very small part of
the article, was he was outside, fell off a high rung of a
(54:11):
ladder, hit the ground, knockedhis head and he was taking
multiple medications bloodpressure, aspirin, warfarin,
non-steroidalanti-inflammatories and a whole
heap of other things.
But it was the omega-3 thatcaused the hemorrhage.
And I'm like really not thefall, not the medications, but
(54:31):
the actual omega-3 it did it.
So I get a bit triggeredsometimes when, um, I sort of
read some abstracts where, youknow, I believe in all research
is useful, but it needs to befactual research.
And that kind of thing was a bitmisleading because the media
picked it up and went with thatomega-3 causes hemorrhaging when
it can if, given the rightsituation, you're a 70 year old
(54:55):
man who fell off a ladder andlanded on your head, so
therefore there's going to beother consequences of having
that, let alone medications.
So, yeah, always read the fullpaper, look into it deeper.
So now, after this podcast, goand read up all the material, go
and have a look and, you know,nourish your own brain with you
(55:15):
know, information ofbiochemistry and genetics and
physiology, because we'relearning more and more every day
and that's what I love aboutnutritional medicine,
naturopathy and what we dobecause we are learning more and
more and the greater theinformation coming out.
It's fantastic and it's justfor me, it's very exciting the
time and place we're at rightnow with what we could do for
(55:38):
our patients and help each otherout as well.
Speaker 1 (55:41):
Dr Brad McKeown, thank you so much for taking us
through.
This is a big topic, I know,but vitamin K2, MK7 today it's
been great having you on.
Thank you so much for joiningus.
Speaker 2 (55:53):
Thank you very much for having me.
Speaker 1 (55:55):
And thank you everyone for joining us today.
Remember we'll put up as manyshow notes as we can.
There's a lot of research here,and you can find out all of the
other podcasts, of course, onthe Designs for Health website.
Thanks so much for joining us.
I'm Andrew Whitfield-Cook.
This is Wellness by Designs.
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